Staph Aureus

Question 1

Characteristics of S. aureus

Answer 1

G+ cocci, facultative anaerobe
Cat+, salt tolerant
Coagulase+
b-hemolytic

Question 2

Where is S. aureus found?

Answer 2

Flora of skin and mucous membranes

Question 3

Cell wall of S. aureus

Answer 3

Capsule with many serotypes, protects from phagocytosis and helps adhesion (PGs, teichoic acid)
Peptidoglycan: more rigid cell wall, endotoxin-like (stimulates complement, IL-1, abscess formation)

Question 4

Teichoic acid, protein A and coagulase

Answer 4

TA: phosphate polymers attached to PG helps attach to fibronectin
PR: FcR of IgG binds IgG before it can bind S. aureus
Coag: clumping factor, binds fibrinogen -> fibrin to build a protein wall and impede immune system/Abs

Question 5

Virulence factors of S. aureus

Answer 5

*Not all produced by all S. aureus

Protein A, coagulase, elastin BP, collagen BP, fibronectin BP, clumping factor, enterotoxin B, TSST-1, alpha toxin, etc.

Question 6

Toxins in S. aureus

Answer 6

5 cytolytic/membrane damaging, 2 exfoliative (SSSS), 8 enterotoxins (superAg, food poisoning), TSST-1 superAg

Question 7

Alpha toxin source and effects

Answer 7

On bacterial chromosomes and plasmids

Causes pores in cell membrane, alters ion balance -> swelling, lysis

Question 8

SSSS (Ritters Disease)

Answer 8

Surface staph infxn of neonates/young children produces A and B exfoliative toxins (serine proteases) to break desmosomes = blisters, sloughing off
*No bacteria in blister fluid b/c toxin-mediated

Question 9

Bullous impetigo

Answer 9

Localized form of SSSS, specific S. aureus strains
Blisters are culture +
In children, highly communicable

Question 10

Enterotoxins (food poisoning)

Answer 10

Stable to heat and GI enzymes; superAgs
Rapid (4h) vom/dia for 24 h w/o fever
In salted meats, custards, ice cream, potato salad - won’t taste spoiled

Question 11

Toxic shock syndrome toxin (TSST-1)

Answer 11

Heat and protease resistant (chromosomal source)

SuperAg, penetrates mucosal barriers to cause systemic effects

Question 12

Mechanism of superantigen & example

Answer 12

Bacterial toxin + MHC-2 and APC = non-specific activation T cells -> massive cytokine release (IL-1,2, TNF-a) -> n/v, fever, malaise -> shock, multiple organ failure, death
*S. aureus & Strep. pyogenes

Question 13

Clinical manifestations of TSST-1

Answer 13

6000/year in US; localized growth followed by release of toxin into blood -> acute fever, hypotension, macular erythematous rash; can be fatal (5%) & high recurrence if AB ineffective
Infected tampon, wounds, surgery, burns

Question 14

S. aureus diseases

Answer 14

SSSS, bullous impetigo, food poisoning, TSS, pyogenic cutaneous infections (impetigo, folliculitis, carb/furuncles), bacteremia, acute endocarditis, pneumonia/ empyema, osteomyelitis, septic arthritis

Question 15

S. epidermidis & saprophyticus diseases

Answer 15

SE: endocarditis (native and prosthetic heart valves), catheter/shunt infections, prosthetic jj infxn
SS: UTI in young women

Question 16

Epidemiology of staph

Answer 16

Ubiquitous, normal flora for many, shedding from skin is most common cause of nosocomial infxn, spread easily (*asepsis)

Question 17

How did MRSA develop?

Answer 17

Picked up MEC-A (mobile gen element, chr cassette) gene through transposition -> modified PBP

Question 18

Lab dx of S. aureus

Answer 18

Grows selectively on 6.5% NaCL agar + mannitol, coagulase+

Question 19

Treatment, prevention, and control of staph

Answer 19

Pen-resistance on plasmid & other resistances common
Vancomycin usually works, but resistance increasing
Aminoglycoside resistance growing

Question 20

Infection control of staph

Answer 20

Hygienic practices, hand washing, tracking by hospitals